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2010 AAOMPT Krista Clark Natural Alternatives to Long-Term NSAID

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2010 AAOMPT Krista Clark Natural Alternatives to Long-Term NSAID Natural Alternatives to Long‐Term NSAID Use Krista J. Clark, PT, FAAOMPT Wellspring Physical Therapy Midway, Utah AAOMPT 2010 AAlnnual CCfonference I have long been interested in integrative healthcare. I see the pendulum swinging to a balance point of approaches that work with modern science and, by science, understanding how the natural age‐old wisdom is useful. As manual physical therapists, because our treatment is natural, we have the knowledge and abilities to bridge these approaches. The focus of this presentation is on delivering information and resources that we as physical therapists can give to patients to improve self advocacy. I have long viewed my roll as a provider of information and data so that people can educate themselves and make more informed decisions regarding their health care. I make this clear to people when these topics are discussed in my clinic. NSIADs • Aspirin, derived from white willow bark has been used since ancient times. Use has been documented as early as 1763. • Indomethicine was released in the 1960s. Ibuprofen as Brufen was released in 1969. • 1988 COX‐2 was indentified in Provo UT. • Action: inhibits prostaglandins • In 1999 16,685 deaths from NAID toxicity, (close to numbers of deaths from Leukemia and AIDS). • Up to 40% of people will have detectable gastric ulcers or some form adverse GI reactions. • Economics: 2001‐$4.8 billion in prescribed drugs and $3 billion OTC analgesics (Includes acetaminophen) were sold. (Laine, Gastroenterology 2001 120:594 ) • Vioxx sales halted in 2004. Data on COX‐2 cardiovascular events was apparent by 2005. • Sean Whelton, MD Georgetown University Hospital Feb. 13, 2009 Effects of antiinflammatory drugs on the progression of osteoarthritis of the knee. LINK Study Group. Longitudinal Investigation of Nonsteroidal Antiinflammatory Drugs in Knee Osteoarthritis. Huskisson EC, Berry H, Gishen P, Jubb RW, Whitehead J. Department of Rheumatology, St. Bartholomew's Hospital, London, UK. J Rheumatol. 1995 Oct;22(10):1941‐6. ¾ 812 patients randomized double blind parallel group ¾ Patients received either indomethacin (Indocin) 25 mg three times daily, tiaprofenic acid (an NSAID, Surgam in the UK) 300 mg twice daily, or matched placebo. ¾ Joint space narrowing was measured by a 6 point grading scale, using radiographs taken with a standardized technique at recruitment and annually thereafter. ¾ RESULTS: Three hundred and seventy six patients completed at least one year of study medication and therefore contributed evaluable results. More than twice as many patients showed deterioration in the indomethacin group as in the placebo group; of 170 available patients at the 3rd interim analysis, 40 of 85 receiving indomethacin had deteriorated compared to 19 of 85 receiving placebo, a statistically significant difference (p = 0. 009). ¾ No statistically significant difference (p = 0.308) was found between tiaprofenic acid and placebo at the 7th interim analysis, the conclusion of the study. ¾ CONCLUSION: Indomethacin increased the rate of radiological deterioration of joint space in patients with OA of the knee; tiaprofenic acid dddid not. The long‐term effects of non‐steroidal anti‐inflammatory drugs in osteoarthritis of the knee: a randomized placebo‐controlled trial D. L. Scott, H. Berry, H. Capell, J. Coppock, et. al. Rheumatology 2000; 39: 1095‐1101© 2000 British Society for Rheumatology ¾ A parallel‐group, randomized, single‐blind trial of patients with knee OA recruited 812 patients from 20 centres; 307 patien ts receidived tiapro fen ic acid (300 mg bd)b.d.), 202 idindome thithacin (25 mg tdt.d.s. ) and 303 matching placebo for up to 5 yr. ¾ At the end of the parallel‐group study, patients receiving tiaprofenic acid or placebo entered a 4‐week blinded cross‐over study of tiaprofenic acid or placebo, both given for 2 weeks. ¾ Assessments were at blibaseline, 4 weeks, then at 6‐month ilintervals for up to 5 yr in the paralle l group study and at 2‐week intervals in the cross‐over study. They comprised pain scores, duration of morning stiffness, patients' global assessments, paracetamol consumption, adverse reactions, withdrawals and functional outcomes. ¾ There were siifitignificant fllfalls in overall pain scores in patien ts receiiiving NSAIDs compared with plblacebo at 4 weeks in the parallel‐group phase. Thereafter there were no advantages favouring active therapy. ¾ In the cross‐over phase, pain scores were significantly lower in patients receiving tiaprofenic acid than placebo. ¾ Potentially severe side‐effects were rare; for example, there were only three cases of gastrointestinal bleeding on NSAIDs. ¾ Conclusions. NSAIDs significantly reduce overall pain over 4 weeks. This short‐term responsiveness is retained, and even after several years of therapy with tiaprofenic acid pain scores increased over 2 weeks when it was chdhanged to plblacebo. ¾ Our results do not show long‐term benefits from the use of NSAIDs in OA and the majority of patients had persisting pain and disability despite therapy. Rheumatology 2000; 39: 1095‐1101, continued Patients who remained on treatment for 12 months or longer not only showed no measurable benefit from active treatment but also had a static clinical picture with unchanging pain levels and durations of morning stiffness (Fig. 2) Is there an association between the use of different types of nonsteroidal antiinflammatory drugs and radiologic progression of osteoarthritis? The RttdRotterdam Stud y. Reijman M, Bierma‐Zeinstra SM, Pols HA, Koes BW, Stricker BH, Hazes JM. Arthritis Rheum. 2005 Oct;52(10):3137‐42. ¾ 1,695 subjects were analyzed, (2,514 hips) and 635 subjects (874 knees) ages 55 years and older from the Rotterdam Study ¾ radiographs of the hip and knee at baseline and followup (mean followup time 6.6 years) were evaluated. ¾ Radiologic OA (ROA) progression was defined as a minimu m increase of 1 in the Kellgren/Lawrence grade or incident joint replacement at followup. ¾ The associations between the different types of NSAIDs and progression of ROA were assessed using multivariate logistic regression analysis. ¾ RESULTS: Those subjects who were receiving diclofenac (Voltaren) >180 days had a 242.4‐ fold increased risk (95% confidence interval [95% CI] 1.0‐6.2) of progression of hip ROA ¾ 3.2‐fold increased risk (95% CI 1.0‐9.9) of knee ROA, compared with those considered short‐term users (diclofenac for 1‐30 days). ¾ These associations were adjusted for age, sex, body mass index, baseline ROA, followup time, and defined daily dosage. ¾ CONCLUSION: These data suggest that diclofenac may induce accelerated progression of hip and knee ROA. ¾ Whether this occurs because of a true deleterious effect on cartilage or because of excessive mechanical loading on a hip following pain relief remains to be investigated. Differential direct effects of cyclo‐oxygenase‐1/2 inhibition on proteoglycan turnover of human osteoarthritic cartilage: an in vitro study. Mastbergen SC, Jansen NW, Bijlsma JW, Lafeber FP. Rheumatology & Clinical Immunology, University Medical Center Utrecht, Utrecht, The Netherlands. Arthritis Res Ther. 2006;8(1):R2. ¾ Comparison of the direct effects of indomethacin, naproxen, aceclofenac and celecoxib on matrix turnover in human OA cartilage tissue. ¾ Human clinically defined OA cartilage from five different donors was exposed for 7 days in culture to indomethacin, naproxen, aceclofenac and celecoxib‐‐agents chosen based on their cyclo‐ oxygenase (COX)‐2 seliilectivity. ¾ As a control, SC‐560 (a selective COX‐1 inhibitor) was used. ¾ Changes in cartilage proteoglycan turnover and prostaglandin E2 production were determined. ¾ OA cartilage exhibited characteristic proteoglycan turnover. Indomethacin further inhibited protlteoglycan synthes is; no siifitignificant effec t of idindome thithacin on protlteoglycan release was fdfound, and proteoglycan content tended to decrease. ¾ Naproxen treatment was not associated with changes in any parameter. ¾ In contrast, aceclofenac and, prominently, celecoxib had beneficial effects on OA cartilage. Both were associated with increased proteoglycan synthesis and normalized release. Importantly, both NSAIDs improved proteoglycan content. ¾ Selective COX‐1 inhibition resulted in adverse effects on all parameters, and prostaglandin E2 production was only mildly inhibited. ¾ NSAIDs with low COX‐2/COX‐1 selectivity exhibit adverse direct effects on OA cartilage, whereas high COX‐2/COX‐1 selective NSAIDs did not show such effects and might even have cartilage reparative properties. Diacerein has a weak effect on the catabolic pathway of human osteoarthritis synovial fibroblast‐‐comparison to its effects on osteoarthritic chondrocytes. Alvarez‐Soria MA, Herrero‐Beaumont G, Sánchez‐Pernaute O, Bellido M, Largo R. Joint and Bone Research Unit, Rheumatology Department,, Avenida Reyes Católicos 2, 28040 Madrid, Spain. Rheumatology (Oxford). 2008 May;47(5):627‐33. Epub 2008 Mar 27 ¾ OBJECTIVES: Synoviocytes play a crucial role in the inflammatory response leading to structural damage in OA. Our aim was to assess the effects of diacere in and NSAIDs on cellular responses of synoviocytes associated with inflammation and structural integrity of cartilage in OA. ¾ METHODS: The effects of diacerein, celecoxib, diclofenac, meloxicam and indomethacin on prostaglandin (PG) E2 production, cyclo‐oxygenase‐2 (COX‐2) protein expression, nitrite levels, presence of MMP‐1 and ‐13, and activation of nuclear factor‐kappaB (NF‐kappaB) were studied on stimulated OA synoviocytes and chondrocytes.
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